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Previous research covering various tissues such as the brain, suggests that the detrimental impact of early-life stress (ELS) on mental health is mediated via epigenetic modifications including DNA methylation. Genes of the hypothalamic\u2013pituitary\u2013adrenal axis\u2014in particular, the glucocorticoid receptor (<jats:italic>hGR<\/jats:italic>) gene\u2014stand out as key targets for ELS. Even though the link between<jats:italic>hGR<\/jats:italic>methylation and either ELS or psychopathology is fairly well established, the mutually dependent relationships between ELS, DNA methylation and psychopathology remain to be uncovered. The specific psychopathology an individual might develop in the aftermath of stressful events can be highly variable, however, most studies investigating<jats:italic>hGR<\/jats:italic>methylation and psychopathology suffer from being limited to a single symptom cluster of mental disorders. Here, we screened volunteers for childhood maltreatment and analyzed whether it associates with<jats:italic>hGR<\/jats:italic>methylation in lymphocytes and a range of measures of psychological ill-health.<jats:italic>hGR<\/jats:italic>methylation in lymphocytes most likely reflects methylation patterns found in the brain and thus provides valuable insights into the etiology of psychopathology. We find the interaction between childhood maltreatment and<jats:italic>hGR<\/jats:italic>methylation to be strongly correlated with an increased vulnerability to psychopathology providing evidence of epigenome \u00d7 environment interactions. Furthermore, our results indicate an additive effect of childhood maltreatment and<jats:italic>hGR<\/jats:italic>methylation in predicting borderline personality disorder (BPD)-associated symptoms, suggesting that the combination of both ELS and DNA methylation that possibly represents unfavorable events experienced even earlier in life poses the risk for BPD.<\/jats:p>","DOI":"10.1038\/tp.2015.63","type":"journal-article","created":{"date-parts":[[2015,6,16]],"date-time":"2015-06-16T16:44:25Z","timestamp":1434473065000},"page":"e571-e571","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":115,"title":["Epigenetic modifications of the glucocorticoid receptor gene are associated with the vulnerability to psychopathology in childhood maltreatment"],"prefix":"10.1038","volume":"5","author":[{"given":"K M","family":"Radtke","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"Schauer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H M","family":"Gunter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"Ruf-Leuschner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J","family":"Sill","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0888-8193","authenticated-orcid":false,"given":"A","family":"Meyer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T","family":"Elbert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2015,5,26]]},"reference":[{"key":"BFtp201563_CR1","doi-asserted-by":"publisher","first-page":"684","DOI":"10.4088\/JCP.08m04235","volume":"70","author":"MH Teicher","year":"2009","unstructured":"Teicher MH, Samson JA, Polcari A, Andersen SL . 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